Recently, a CRB trial evaluated the ability of IL-1alpha to ameliorate the thrombocytopenia associated with the administration of 800 mg/m2 of CBDCA. The 10 pts. treated with IL-1alpha, 0.3 microgram/kg, showed significantly faster platelet recovery than 8 pts. in a control group who receive CBDCA alone. However, a very high rate of hypotension was associated with administration of 0.3 microgram/kg of IL-1alpha to these pts. Unfortunately, treatment with lower doses of IL-1alpha had no significant effect on platelet nadir or recovery. 1 potential solution would be to administer an agent that could reverse or prevent the arteriolar smooth muscle relaxation that follows IL-1alpha treatment. Successful control of IL-1alpha-induced hypotension might have implications for immunotherapy with other cytokines with vasodilatory action (e.g., IL-2 and TNF) and could also be an important step in defining a new means to reverse the shock associated with life-threatening sepsis. It has recently been demonstrated that in vivo administration of endotoxin, TNF, IL-1, and IL-2 prompt a profound increase in generation of nitric oxide, the common endogenous mediator of vasodilation. In vitro studies have demonstrated that methylene blue (MB) can reverse the arterial relaxation associated with nitric oxide production. In this protocol, pts. will receive CBDCA followed by IL-1alpha given at fixed high doses. Escalating doses of MB will then be tested as a means to reverse mediated hypotension.